Establishment of a new conditionally immortalized human brain microvascular endothelial cell line retaining an in vivo blood-brain barrier function

2010 ◽  
Vol 225 (2) ◽  
pp. 519-528 ◽  
Author(s):  
Yasuteru Sano ◽  
Fumitaka Shimizu ◽  
Masaaki Abe ◽  
Toshihiko Maeda ◽  
Yoko Kashiwamura ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Human Brain ◽  
Cell Line ◽  
Blood Brain Barrier ◽  
Barrier Function ◽  
Brain Barrier ◽  
Microvascular Endothelial Cell ◽  
Brain Microvascular Endothelial Cell ◽  
Endothelial Cell Line

Stable human brain microvascular endothelial cell line retaining its barrier-specific nature independent of the passage number

2012 ◽  
Vol 4 (1) ◽  
pp. 92-103 ◽  
Author(s):  
Yasuteru Sano ◽  
Yoko Kashiwamura ◽  
Masaaki Abe ◽  
Le-Ha Dieu ◽  
Jörg Huwyler ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Human Brain ◽  
Cell Line ◽  
Microvascular Endothelial Cell ◽  
Brain Microvascular Endothelial Cell ◽  
Specific Nature ◽  
Endothelial Cell Line ◽  
Passage Number ◽  
Microvascular Endothelial

scholarly journals Human Brain Endothelial CXCR2 is Inflammation-Inducible and Mediates CXCL5- and CXCL8-Triggered Paraendothelial Barrier Breakdown

2019 ◽  
Vol 20 (3) ◽  
pp. 602 ◽  
Author(s):  
Axel Haarmann ◽  
Michael Schuhmann ◽  
Christine Silwedel ◽  
Camelia-Maria Monoranu ◽  
Guido Stoll ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Tight Junction ◽  
Human Brain ◽  
Blood Brain Barrier ◽  
Barrier Function ◽  
Morphological Changes ◽  
Brain Barrier ◽  
Microvascular Endothelial Cell ◽  
Inflammatory Conditions ◽  
Blood Brain

Chemokines (C-X-C) motif ligand (CXCL) 5 and 8 are overexpressed in patients with multiple sclerosis, where CXCL5 serum levels were shown to correlate with blood–brain barrier dysfunction as evidenced by gadolinium-enhanced magnetic resonance imaging. Here, we studied the potential role of CXCL5/CXCL8 receptor 2 (CXCR2) as a regulator of paraendothelial brain barrier function, using the well-characterized human cerebral microvascular endothelial cell line hCMEC/D3. Low basal CXCR2 mRNA and protein expression levels in hCMEC/D3 were found to strongly increase under inflammatory conditions. Correspondingly, immunohistochemistry of brain biopsies from two patients with active multiple sclerosis revealed upregulation of endothelial CXCR2 compared to healthy control tissue. Recombinant CXCL5 or CXCL8 rapidly and transiently activated Akt/protein kinase B in hCMEC/D3. This was followed by a redistribution of tight junction-associated protein zonula occludens-1 (ZO-1) and by the formation of actin stress fibers. Functionally, these morphological changes corresponded to a decrease of paracellular barrier function, as measured by a real-time electrical impedance-sensing system. Importantly, preincubation with the selective CXCR2 antagonist SB332235 partially prevented chemokine-induced disturbance of both tight junction morphology and function. We conclude that human brain endothelial CXCR2 may contribute to blood–brain barrier disturbance under inflammatory conditions with increased CXCL5 and CXCL8 expression, where CXCR2 may also represent a novel pharmacological target for blood–brain barrier stabilization.

scholarly journals Human brain microvascular endothelial cell pairs model tissue-level blood–brain barrier function

2020 ◽  
Vol 12 (3) ◽  
pp. 64-79
Author(s):  
Blakely B O’Connor ◽  
Thomas Grevesse ◽  
John F Zimmerman ◽  
Herdeline Ann M Ardoña ◽  
Jorge A Jimenez ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Human Brain ◽  
Blood Brain Barrier ◽  
Barrier Function ◽  
Cytoskeletal Proteins ◽  
Fiber Formation ◽  
Brain Barrier ◽  
Actin Stress Fiber ◽  
Barrier Permeability ◽  
Blood Brain

Abstract The blood–brain barrier plays a critical role in delivering oxygen and nutrients to the brain while preventing the transport of neurotoxins. Predicting the ability of potential therapeutics and neurotoxicants to modulate brain barrier function remains a challenge due to limited spatial resolution and geometric constraints offered by existing in vitro models. Using soft lithography to control the shape of microvascular tissues, we predicted blood–brain barrier permeability states based on structural changes in human brain endothelial cells. We quantified morphological differences in nuclear, junction, and cytoskeletal proteins that influence, or indicate, barrier permeability. We established a correlation between brain endothelial cell pair structure and permeability by treating cell pairs and tissues with known cytoskeleton-modulating agents, including a Rho activator, a Rho inhibitor, and a cyclic adenosine monophosphate analog. Using this approach, we found that high-permeability cell pairs showed nuclear elongation, loss of junction proteins, and increased actin stress fiber formation, which were indicative of increased contractility. We measured traction forces generated by high- and low-permeability pairs, finding that higher stress at the intercellular junction contributes to barrier leakiness. We further tested the applicability of this platform to predict modulations in brain endothelial permeability by exposing cell pairs to engineered nanomaterials, including gold, silver–silica, and cerium oxide nanoparticles, thereby uncovering new insights into the mechanism of nanoparticle-mediated barrier disruption. Overall, we confirm the utility of this platform to assess the multiscale impact of pharmacological agents or environmental toxicants on blood–brain barrier integrity.

Development of immortalized human cerebromicrovascular endothelial cell line as an in vitro model of the human blood–brain barrier

1997 ◽  
Vol 11 (13) ◽  
pp. 1187-1197 ◽  
Author(s):  
Arumugam Muruganandam ◽  
Leonie Moorhouse Herx ◽  
Robert Monette ◽  
Jon P. Durkin ◽  
Danica B. Stanimirovic
Keyword(s):  
Endothelial Cell ◽  
Cell Line ◽  
Blood Brain Barrier ◽  
Human Blood ◽  
In Vitro Model ◽  
Brain Barrier ◽  
Endothelial Cell Line ◽  
Blood Brain ◽  
Vitro Model
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